Non-specific proctitis is considered to be a localized form of ulcerdrive colitis with identical histopathological findings (cf. Dennard-Jones, J E et al, Gut 1962, 3, p. 201-208). Ulcerative colitis always starts with rectal inflammation, but only one tenth of the proctitis patients will develop colohio disease. Recently damage and regeneration of peptide-containing neurons were observed in ulcerdrive colitis, suggesting damage of these neurons as a primary event (cf, Koch T R et al, Inflammatory Bowel Disease: Current status and future approach. Elsevier Science Publishers BV 1988, p. 25-30). Relatively few studies on inflammatory bowel disease have dealt with the influence of stress on intestinal function at the cellular level. Hyperplasia of the mucosal adrenergic innervation and reduction of the number of rectal enterochromaffin cells were first demonstrated in ulcerdrive colitis by Kyoola et al in Scand J Gastroent. 1977, 12, p. 363-367 using the Hillarp-Falck technique (cf. Corrodi H., Jonsson Cr., S. Histochem Cytochem 1967, 15, p. 65-78). Lymphocytes and plasma cells accumulate in the lamina proprid and together with polymorphnuclear cells crypt abscesses may form. Subsets of lymphocytes invade the inflamed mucosa, i.e. the suppressor-cytotoxic phenotype, (OKT.sub.8), resides within the epithelium and the helper phenotype ( OKT.sub.4), within the proprid (cf. Selby W S et al., Gut 1984, 25, p. 32-40).